Function of the Cerebellum

• The cerebellum contains as many neurons as the rest of the

brain combined.
• Control motor function that has afferent and efferent
connections to the cortex and periphery
• The cerebellum is involved in the planning, execution. And
control of movement and is responsible for motor adaptation to
new movement sequences (motor learning).
• It also cooperates with higher centers to control attention,
How is it that the cerebellum can be so important when it has no
direct ability to cause muscle contraction?

• The answer is that it helps sequence the motor activities and

also monitors and makes corrective adjustments in the body’s
motor activities while they are being executed so that they will
conform to the motor signals directed by the cerebral motor
cortex and other parts of the brain.
• The cerebellum also aids the cerebral cortex in planning the
next sequential movement a fraction of a second in advance
while the current movement is still being executed
• Also, it learns by its mistakes—that is, if a movement does not
occur exactly as intended, the cerebellar circuit learns to make
a stronger or weaker movement the next time.
Anatomical and Functional Areas of the Cerebellum
• The nervous system uses the cerebellum to
coordinate motor control functions at three
levels:
• 1. The vestibulocerebellum. This level consists
principally of the small flocculonodular
cerebellar lobes that lie under the posterior
cerebellum and adjacent portions of the
vermis. It provides neural circuits for most of
the body’s equilibrium movements.
• The spinocerebellum. This level consists of
most of the vermis of the posterior and
anterior cerebellum plus the adjacent
intermediate zones on both sides of the
vermis. It provides the circuitry for
coordinating mainly movements of the distal
portions of the limbs, especially the hands and
fingers.
• 3. The cerebrocerebellum. This level consists of the
large lateral zones of the cerebellar hemispheres,
lateral to the intermediate zones. It receives virtually all
its input from the cerebral motor cortex and adjacent
premotor and somatosensory cortices of the cerebrum.
It transmits its output information in the upward
direction back to the brain, functioning in a feedback
manner with the cerebral cortical sensorimotor system
to plan sequential voluntary body and limb
movements. These movements are planned as much as
tenths of a second in advance of the actual
movements. This process is called development of
“motor imagery” of movements to be performed.
 Clinical Abnormalities of the
Cerebellum
• Destruction of small portions of the lateral cerebellar
cortex seldom causes detectable abnormalities in
motor function. In fact, several months after as much
as one half of the lateral cerebellar cortex on one side
of the brain has been removed, if the deep cerebellar
nuclei are not removed along with the cortex, the
motor functions of the animal appear to be almost
normal as long as the animal performs all movements
slowly. Thus, the remaining portions of the motor
control system are capable of compensating to a great
extent for loss of parts of the cerebellum.
• Dysmetria and Ataxia
Two of the most important symptoms of cerebellar disease
are dysmetria and ataxia. In the absence of the
cerebellum, the subconscious motor control system
cannot predict how far movements will go. Therefore,
the movements ordinarily overshoot their intended
mark; then the conscious portion of the brain
overcompensates in the opposite direction for the
succeeding compensatory movement. This effect is
called dysmetria, and it results in uncoordinated
movements that are called ataxia. Dysmetria and ataxia
can also result from lesions in the spinocerebellar
tracts because feedback information from the moving
parts of the body to the cerebellum is essential for
cerebellar timing of movement termination.
• Past Pointing
Past pointing means that in the absence of the
cerebellum, a person ordinarily moves the hand
or some other moving part of the body
considerably beyond the point of intention. This
movement results from the fact that normally the
cerebellum initiates most of the motor signal that
turns off a movement after it is begun; if the
cerebellum is not available to initiate this motor
signal, the movement ordinarily goes beyond the
intended mark. Therefore, past pointing is
actually a manifestation of dysmetria.
• Failure of Progression
Dysdiadochokinesia—Inability to Perform Rapid Alternating
Movements. When the motor control system fails to predict where
the different parts of the body will be at a given time, it “loses”
perception of the parts during rapid motor movements. As a result,
the succeeding movement may begin much too early or much too
late, so no orderly “progression of movement” can occur. One can
demonstrate this effect readily by having a patient with cerebellar
damage turn one hand upward and downward at a rapid rate. The
patient rapidly “loses” all perception of the instantaneous position of
the hand during any portion of the movement. As a result, a series of
stalled attempted but jumbled movements occurs instead of the
normal coordinate upward and downward motions. This condition is
called dysdiadochokinesia.
• Dysarthria—Failure of Progression in Talking. Another
example in which failure of progression occurs is in talking
because the formation of words depends on rapid and orderly
succession of individual muscle movements in the larynx,
mouth, and respiratory system. Lack of coordination among
these structures and the inability to adjust in advance either the
intensity of sound or the duration of each successive sound
causes jumbled vocalization, with some syllables loud, some
weak, some held for long intervals, and some held for short
intervals, with resultant speech that is often unintelligible. This
condition is called dysarthria.
• Intention Tremor. When a person who has lost the
cerebellum performs a voluntary act, the
movements tend to oscillate, especially when they
approach the intended mark, first overshooting the
mark and then vibrating back and forth several
times before settling on the mark. This reaction is
called an intention tremor or an action tremor,
and it results from cerebellar overshooting and
failure of the cerebellar system to “damp” the
motor movements.
• Cerebellar Nystagmus—Tremor of the Eyeballs.
Cerebellar nystagmus is tremor of the eyeballs that
usually occurs when one attempts to fixate the eyes on a
scene to one side of the head. This off-center type of
fixation results in rapid, tremulous movements of the
eyes rather than steady fixation, and it is another
manifestation of the failure of damping by the
cerebellum. It occurs especially when the
flocculonodular lobes of the cerebellum are damaged;
in this instance, it is also associated with loss of
equilibrium because of dysfunction of the pathways
through the flocculonodular cerebellum from the
semicircular ducts.
• Hypotonia—Decreased Tone of the Musculature
Loss of the deep cerebellar nuclei, particularly of
the dentate and interposed nuclei, causes
decreased tone of the peripheral body musculature
on the side of the cerebellar lesion. The hypotonia
results from loss of cerebellar facilitation of the
motor cortex and brain stem motor nuclei by tonic
signals from the deep cerebellar nuclei.
THE BASAL GANGLIA AND THEIR
MOTOR FUNCTIONS
They begin mainly in the premotor and supplementary
areas of the motor cortex and in the somatosensory
areas of the sensory cortex. Next they pass to the
putamen (mainly bypassing the caudate nucleus), then to
the internal portion of the globus pallidus, and next to
the ventroanterior and ventrolateral relay nuclei of the
thalamus, and they finally return to the cerebral primary
motor cortex and to portions of the premotor and
supplementary cerebral areas closely associated with the
primary motor cortex. Thus, the putamen circuit has its
inputs mainly from the parts of the brain adjacent to the
primary motor cortex but not much from the primary
motor cortex itself. Then its outputs do go mainly back to
the primary motor cortex or closely associated premotor
and supplementary cortex. Functioning in close
association with this primary putamen circuit are
ancillary circuits that pass from the putamen through the
external globus pallidus, the subthalamus, and the
substantia nigra—finally returning to the motor cortex by
way of the thalamus.
 Abnormal Function in the Putamen
Circuit: Athetosis, Hemiballismus, and
Chorea
• When a portion of the circuit is damaged or blocked, certain patterns
of movement become severely abnormal. For instance, lesions in the
globus pallidus frequently lead to spontaneous and often continuous
writhing movements of a hand, an arm, the neck, or the face. These
movements are called athetosis.
• A lesion in the subthalamus often leads to sudden flailing
movements of an entire limb, a condition called hemiballismus.
• Multiple small lesions in the putamen lead to flicking movements in
the hands, face, and other parts of the body, called chorea.
• Lesions of the substantia nigra lead to the common and extremely
severe disease of rigidity, akinesia, and tremors known as
Parkinson’s disease, which we discuss in more detail later in this
chapter.
 ROLE OF THE BASAL GANGLIA FOR COGNITIVE
CONTROL OF SEQUENCES OF MOTOR PATTERNS—
THE CAUDATE CIRCUIT

• Example:a person seeing a lion approach and then responding

instantaneously and automatically by (1) turning away from
the lion, (2) beginning to run, and (3) even attempting to climb
a tree. Without the cognitive functions, the person might not
have the instinctive knowledge, without thinking for too long a
time, to respond quickly and appropriately. Thus, cognitive
control of motor activity determines subconsciously, and
within seconds, which patterns of movement will be used
together to achieve a complex goal that might itself last for
many seconds.
• Clinical Syndromes Resulting From Damage to the Basal Ganglia
• Parkinson’s disease, which is also known as paralysis agitans, results from widespread destruction of the
portion of the substantia nigra (the pars compacta) that sends dopamine-secreting nerve fibers to the
caudate nucleus and putamen. The disease is characterized by (1) rigidity of much of the musculature of
the body; (2) involuntary tremor of the involved areas even when the person is resting at a fixed rate of
three to six cycles per second; (3) serious difficulty in initiating movement, called akinesia; (4) postural
instability caused by impaired postural reflexes, leading to poor balance and falls; and (5) other motor
symptoms, including dysphagia (impaired ability to swallow), speech disorders, gait disturbances, and
fatigue.
• The causes of these abnormal motor effects are unknown. However, the dopamine secreted in the caudate
nucleus and putamen is an inhibitory transmitter; therefore, destruction of the dopaminergic neurons in
the substantia nigra of the parkinsonian patient theoretically would allow the caudate nucleus and
putamen to become overly active and possibly cause continuous output of excitatory signals to the
corticospinal motor control system. These signals could overly excite many or all of the muscles of the
body, thus leading to rigidity. Some of the feedback circuits might easily oscillate because of high
feedback gains after loss of their inhibition, leading to the tremor of Parkinson’s disease. This tremor is
quite different from that of cerebellar disease because it occurs during all waking hours and therefore is
an involuntary tremor, in contradistinction to cerebellar tremor, which occurs only when the person
performs intentionally initiated movements and therefore is called intention tremor.
• The akinesia that occurs in Parkinson’s disease is often much more distressing to the patient than are the
symptoms of muscle rigidity and tremor, because a person with severe parkinsonism must exert the
highest degree of concentration to perform even the simplest movement. The mental effort, even mental
anguish, that is necessary to make the desired movements is often at the limit of the patient’s willpower.
Then, when the movements do occur, they are usually stiff and staccato in character instead of smooth.
The cause of this akinesia is still speculative. However, dopamine secretion in the limbic system,
especially in the nucleus accumbens, is often decreased, along with its decrease in the basal ganglia.
• Treatment With L-Dopa. Administration of the drug L-dopa to
patients with Parkinson’s disease usually ameliorates many of
the symptoms, especially the rigidity and akinesia. The reason
for this amelioration is believed to be that L-dopa is converted
in the brain into dopamine, and the dopamine then restores the
normal balance between inhibition and excitation in the
caudate nucleus and putamen. Administration of dopamine
does not have the same effect because dopamine has a
chemical structure that will not allow it to pass through the
blood-brain barrier; the slightly different structure of L-dopa
allows it to pass through this barrier.
 Huntington’s Disease (Huntington’s Chorea)

• Huntington’s disease is a autosomal dominant hereditary disorder

that usually begins causing symptoms at age 30 to 40 years. It is
characterized at first by flicking movements in individual muscles
and then progressive severe distortional movements of the entire
body. In addition, severe dementia develops along with the motor
dysfunctions.
• The abnormal movements of Huntington’s disease are believed to be
caused by the loss of most of the cell bodies of the GABA-secreting
neurons in the caudate nucleus and putamen and the loss of
acetylcholine-secreting neurons in many parts of the brain. The axon
terminals of the GABA neurons normally inhibit portions of the
globus pallidus and substantia nigra. This loss of inhibition is
believed to allow spontaneous outbursts of globus pallidus and
substantia nigra activity that cause the distortional movements.
• Dementia in persons with Huntington’s disease probably does
not result from the loss of GABA neurons but from the loss of
acetylcholine-secreting neurons, perhaps especially in the
thinking areas of the cerebral cortex.
• The abnormal gene that causes Huntington’s disease has been
found; it has a many-times-repeating codon, CAG, that codes
for multiple extra glutamine amino acids in the molecular
structure of an abnormal neuronal cell protein called
huntingtin that causes the symptoms. How this protein causes
the disease effects is now the question for major research
efforts.
 Cerebrospinal fluid is formed at a rate
of about 500 milliliters each day,
which is three to four times as much as
the total volume of fluid in the entire
cerebrospinal fluid system. About two
thirds or more of this fluid originates
as secretion from the choroid plexuses
in the four ventricles, mainly in the two
lateral ventricles. Additional small
amounts of fluid are secreted by the
ependymal surfaces of all the
ventricles and by the arachnoidal
membranes. A small amount comes
from the brain through the
perivascular spaces that surround the
blood vessels passing through the
brain.
• The main channels of fluid flow from the choroid
plexuses and then through the cerebrospinal fluid
system. The fluid secreted in the lateral ventricles passes
first into the third ventricle; then, after addition of
minute amounts of fluid from the third ventricle, it flows
downward along the aqueduct of Sylvius into the fourth
ventricle, where still another minute amount of fluid is
added. Finally, the fluid passes out of the fourth
ventricle through three small openings, two lateral
foramina of Luschka and a midline foramen of
Magendie, entering the cisterna magna, a fluid space
that lies behind the medulla and beneath the cerebellum.
• The cisterna magna is continuous with the subarachnoid
space that surrounds the entire brain and spinal cord.
Almost all the cerebrospinal fluid then flows upward
from the cisterna magna through the subarachnoid
spaces surrounding the cerebrum. From here, the fluid
flows into and through multiple arachnoidal villi that
project into the large sagittal venous sinus and other
venous sinuses of the cerebrum. Thus, any extra fluid
empties into the
• venous blood through pores of these villi.